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Induction of Ets‐1 in endothelial cells during reendothelialization after denuding injury
Author(s) -
Tanaka Katsuhiro,
Oda Nobuyuki,
Iwasaka Chika,
Abe Mayumi,
Sato Yasufumi
Publication year - 1998
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199808)176:2<235::aid-jcp2>3.0.co;2-p
Subject(s) - p38 mitogen activated protein kinases , mapk/erk pathway , microbiology and biotechnology , kinase , protein kinase a , umbilical vein , endothelial stem cell , chemistry , biology , in vitro , biochemistry
Ets‐1, a transcription factor, is induced in endothelial cells (ECs) during angiogenesis. Here, we investigated the expression of Ets‐1 during reendothelialization. When a confluent monolayer of human umbilical vein endothelial cell line, ECV304, was denuded, ECV304 at the wound edge expressed Ets‐1. An immunohistochemical analysis revealed that Ets‐1 accumulated in migrating cells at the wound edge and returned to basal level when reendothelialization was accomplished. This induction of Ets‐1 could be reproduced in in vivo denudation of rat aortic endothelium by a balloon catheter. The induction of Ets‐1 in ECs after denudation was regulated transcriptionally, and humeral factors released from injured ECs might not be responsible. Mitogen‐activated protein kinase (MAPK) activities were investigated to explore the mechanism of this induction. Although extracellular signal‐regulated protein kinase 1/2 (ERK1/2), c‐Jun N‐terminal kinase 1 (JNK1), and p38 were activated after denudation, the activation of ERK1 and p38 was more rapid and prominent. PD98059, a specific MAPK/ERK kinase (MEK) 1 inhibitor, did not affect the induction of ets ‐1 mRNA, whereas SB203580, a specific p38 inhibitor, almost completely abrogated its induction. These results indicate that Ets‐1 is induced in ECs after denudation through activation of p38. This induction of Ets‐1 may be relevant for reendothelialization by regulating the expression of certain genes. J. Cell. Physiol. 176:235–244, 1998. © 1998 Wiley‐Liss, Inc.